Kato J, Kohgo Y, Sugawara N, Katsuki S, Shintani N, Fujikawa K, Miyazaki E, Kobune M, Takeichi N, Niitsu Y
Department of Internal Medicine (Section 4), Sapporo Medical College.
Jpn J Cancer Res. 1993 Mar;84(3):219-22. doi: 10.1111/j.1349-7006.1993.tb02859.x.
The LEC (Long-Evans cinnamon) rat is a mutant strain displaying hereditary hepatitis and spontaneous hepatocellular carcinoma, and shows abnormal hepatic copper accumulation similar to that occurring in Wilson's disease. We evaluated the iron metabolism of LEC rats compared to LEA (Long-Evans agouti) rats. Hepatic iron and ferritin concentrations were remarkably increased depending on age in LEC rats but not in LEA rats. Increased hepatic iron is normally associated with decreased serum transferrin and total iron binding capacity in hepatic iron overload. In LEC rats, however, both serum transferrin and total iron binding capacity increased with increasing hepatic iron. This increase of serum transferrin and hepatic iron may be an additional important factor contributing to liver injury in LEC rats.
LEC(Long-Evans肉桂色)大鼠是一种突变品系,表现出遗传性肝炎和自发性肝细胞癌,并且显示出与威尔逊病中出现的情况类似的肝脏铜异常蓄积。我们将LEC大鼠与LEA(Long-Evans刺鼠色)大鼠相比,评估了LEC大鼠的铁代谢情况。LEC大鼠肝脏中的铁和铁蛋白浓度随年龄显著增加,而LEA大鼠则不然。在肝脏铁过载时,肝脏铁增加通常与血清转铁蛋白和总铁结合力降低相关。然而,在LEC大鼠中,血清转铁蛋白和总铁结合力均随肝脏铁含量增加而升高。血清转铁蛋白和肝脏铁的这种增加可能是导致LEC大鼠肝损伤的另一个重要因素。